Abstract
Previous work showed that about 85% of stress-induced mutations associated with DNA double-strand break repair in carbon-starved Escherichia coli result from error-prone DNA polymerase IV (Pol IV) (DinB) and that the mutagenesis is controlled by the RpoS stress response, which upregulates dinB. We report that the remaining mutagenesis requires high-fidelity Pol II, and that this component also requires RpoS. The results identify a second DNA polymerase contributing to stress-induced mutagenesis and show that RpoS promotes mutagenesis by more than the simple upregulation of dinB.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Bacterial Proteins / genetics
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Bacterial Proteins / metabolism*
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DNA Polymerase II / genetics
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DNA Polymerase II / metabolism*
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DNA Polymerase beta / genetics
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DNA Polymerase beta / metabolism*
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DNA Repair* / genetics
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Escherichia coli / enzymology*
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Escherichia coli / genetics*
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Escherichia coli Proteins / genetics
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Escherichia coli Proteins / metabolism*
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Mutagenesis
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Mutation / genetics
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Sigma Factor / genetics
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Sigma Factor / metabolism*
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Signal Transduction / genetics
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Signal Transduction / physiology*
Substances
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Bacterial Proteins
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Escherichia coli Proteins
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Sigma Factor
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sigma factor KatF protein, Bacteria
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DNA Polymerase II
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DNA Polymerase beta